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  Transcription factor EBF1 is essential for the maintenance of B cell identity and prevention of alternative fates in committed cells

Nechanitzky, R., Akbas, D., Scherer, S., Györy, I., Hoyler, T., Ramamoorthy, S., et al. (2013). Transcription factor EBF1 is essential for the maintenance of B cell identity and prevention of alternative fates in committed cells. Nature Immunology, 14, 867-875.

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 Creators:
Nechanitzky, Robert1, Author              
Akbas, Duygu1, Author              
Scherer, Stefanie1, Author              
Györy, Ildiko1, Author              
Hoyler, Thomas, Author
Ramamoorthy, Senthilkumar2, Author
Diefenbach, Andreas, Author
Grosschedl, Rudolf1, Author              
Affiliations:
1Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243641              
2Max Planck Society, ou_persistent13              

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 Abstract: The transcription factors EBF1 and Pax5 have been linked to activation of the B cell lineage program and irreversible loss of alternative lineage potential (commitment), respectively. Here we conditionally deleted Ebf1 in committed pro-B cells after transfer into alymphoid mice. We found that those cells converted into innate lymphoid cells (ILCs) and T cells with variable-diversity-joining (VDJ) rearrangements of loci encoding both B cell and T cell antigen receptors. As intermediates in lineage conversion, Ebf1-deficient CD19+ cells expressing Pax5 and transcriptional regulators of the ILC and T cell fates were detectable. In particular, genes encoding the transcription factors Id2 and TCF-1 were bound and repressed by EBF1. Thus, both EBF1 and Pax5 are required for B lineage commitment by repressing distinct and common determinants of alternative cell fates.

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Language(s): eng - English
 Dates: 2013-08
 Publication Status: Published in print
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 Table of Contents: -
 Rev. Type: Peer
 Identifiers: eDoc: 676527
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Title: Nature Immunology
Source Genre: Journal
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Pages: - Volume / Issue: 14 Sequence Number: - Start / End Page: 867 - 875 Identifier: -